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Free download. Book file PDF easily for everyone and every device. You can download and read online Filoviruses: A Compendium of 40 Years of Epidemiological, Clinical, and Laboratory Studies file PDF Book only if you are registered here. And also you can download or read online all Book PDF file that related with Filoviruses: A Compendium of 40 Years of Epidemiological, Clinical, and Laboratory Studies book. Happy reading Filoviruses: A Compendium of 40 Years of Epidemiological, Clinical, and Laboratory Studies Bookeveryone. Download file Free Book PDF Filoviruses: A Compendium of 40 Years of Epidemiological, Clinical, and Laboratory Studies at Complete PDF Library. This Book have some digital formats such us :paperbook, ebook, kindle, epub, fb2 and another formats. Here is The CompletePDF Book Library. It's free to register here to get Book file PDF Filoviruses: A Compendium of 40 Years of Epidemiological, Clinical, and Laboratory Studies Pocket Guide.

Kuhn explains the structure and replication of the filoviruses, with the actual role of each gene of the virus from entry into the target cells to production of infectious virus. He lists diagnosis techniques and experimental treatments of the Marburg and Ebola diseases, from the traditional healers to the molecular antisenses RNA approaches.

In the past 10 years, preexposure and postexposures vaccinations have resulted in tremendous progress in schedules, routes of administration, and more importantly, understanding mechanisms of action. Lack or efficacy of inactivated and live-attenuated constructs is reviewed of all testing in available animal models. This book is not, and is not supposed to be, a critical review of the literature but is rather a compilation of all known information on filoviruses by subject matter experts that is presented for filovirologists.

Review ARTICLE

Nonspecialist virologists, scientists, epidemiologists, clinicians, and students interested in the subject will also find the book useful, but they will have to digest and analyze the information and then weigh the values and relevance of this incredible compendium of data. Suggested citation for this article: Rollin P. Filoviruses: a compendium of 40 years of epidemiological, clinical, and laboratory studies [book review].

Emerg Infect Dis [serial on the Internet]. E-book: www.

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National Center for Biotechnology Information , U. Journal List Emerg Infect Dis v. Emerg Infect Dis. Reviewed by Pierre Rollin. Author information Article notes Copyright and License information Disclaimer. Filovirus outbreaks in Africa. Ultrastructure and structure of filovirus virons. Particles of various forms are visualized by negative staining by uracyl acetate a, b.

Schematic representation of a filovirion indicating protein composition, the tubular nucleocapsid and the surface spikes d. From Kuhn JH. In: Calisher CH editor. Springer, Wien, NewYork; Haemorrhagic manifestations vary in severity and location, and often include skin rash, conjunctival injection, nosebleeds, melaena, haematemesis and bleeding at venepuncture sites. In fatal cases the symptoms and haemorrhaging rapidly become severe, and death generally ensues in a context of tachypnoea, coma and shock.

More specific signs, associated with transient persistence of the virus in immunologically protected sites such as the eyes and testicles have been reported during the early stages of recovery. Biological parameters are not specific for filovirus infection and most data come from experimentally infected animals [ 33 , 34 ]. The prothrombin time is always prolonged and fibrin split products are often detected, indicating disseminated intravascular coagulation [ 35 , 36 ]. Hence, the disease burden of filovirus infection in Africa is extremely small compared with other infectious diseases and malnutrition.

As said previously, the first MARV outbreak occurred in Europe and was associated with 31 cases, including 25 primary cases i. Since then, only sporadic cases have been reported, in South Africa in three cases, one death and in Kenya in two cases, one death and one fatal case [ 31 , 38 , 39 ]. Most patients worked in underground gold mines.

Responding to Outbreaks

The Durba outbreak was characterized by the circulation of multiple viral strains, pointing to multiple independent introductions from the unknown natural reservoir [ 29 , 40 , 41 ]. Complete genomic characterization showed that the culprit strain was closely related to previous East African isolates [ 42 ]. Finally, small MARV outbreaks occurred in western Uganda in and among workers in lead and gold mines of the Kitaka Cave near Ibanda village [ 43 , 44 ].


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Two of the six victims died. In Sudan, the outbreak was centred in the Nzara and Maridi and was responsible for cases. The only case caused by CIEBOV occurred in , when an ethnologist sickened a few days after autopsying a chimpanzee found dead in the Tai national park in Ivory Coast [ 47 - 49 ]. Despite the deployment of more sophisticated scientific and medical resources than those available in , this outbreak was as large as the outbreak, probably because it affected a town with several hundred thousand inhabitants.

In total, these outbreaks involved cases and caused 75 deaths. The second outbreak hit the village of Mayibout, located south of Mekouka, among children who had carried and butchered a chimpanzee carcass found in the forest. Fifteen cases and 11 deaths were recorded in Libreville, the capital of Gabon, and a South African nurse was infected by a Gabonese physician who had travelled to Johannesburg.

Ebola and Marburg Hemorrhagic Fevers: Neglected Tropical Diseases?

RC was again affected twice in respectively and 35 cases, and and 29 deaths , and then in at Etoumbi, where only 11 cases nine fatalities were reported. Two outbreaks of Sudan Ebola virus also occurred during this period. One hit Uganda in , comprised three foci and was the largest of all recorded EBOV outbreaks, causing deaths among its victims [ 59 , 60 ]. There were 17 cases and seven deaths [ 61 - 63 ]. The monkeys developed a haemorrhagic disease associated with high lethality, and subsequent outbreaks among cynomolgus monkeys were reported in animal facilities in Texas, USA, Italy and the Philippines [ 39 , 65 - 68 ].

Although no humans fell sick during these episodes, several monkey handlers in the United States and in the Philippines were shown to have seroconverted [ 69 , 70 ].

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This complex is involved in transcription and replication [ 72 - 74 ]. The matrix proteins VP40 and VP24 are linked to the ribonucleoprotein complex at the inner surface of the lipid bilayer of the viral envelope, which is derived from the host cell. VP40 and VP24 are involved in viral nucleocapsid formation, viral budding or assembly, and host range determination [ 72 , 75 - 82 ]. The viral envelope contains only the glycoproteins, organized as trimeric spikes Fig. The role of sGP is poorly understood. Our knowledge of filovirus distribution and diversity may be limited because EBOV and MARV have only been identified and characterized in sick or dead humans and animals [ 40 , 42 , 43 , 53 - 56 , 64 , 68 , 71 , - ].

Filoviruses: A Compendium of 40 Years of Epidemiological, Clinical, and Laboratory Studies

Remotely sensed data and niche ecologic modelling suggest that filoviruses may circulate within a much wider region than their outbreak areas [ - ]. The seroprevalence was significantly higher in forested areas These results are consistent with previous reports of seroprevalence rates ranging from 1.

More convincingly, two recent small serosurveys, based on the same ELISA as the one we used, have shown high antibody prevalence in some forested regions of Central Africa. Indeed, a 9. Such high seroprevalence rates indicate a high level of ZEBOV circulation in the tropical rain forest environment and suggest that human rural populations are highly exposed to the virus, with mild or asymptomatic infection by outbreak strains [ ] or less pathogenic strains, or simple exposure to inert viral particles.

Filovirus haemorrhagic fevers are typical zoonotic diseases transmitted accidentally by direct contact with live or dead animals. In addition to its high pathogenicity for humans, ZEBOV has caused massive outbreaks among gorillas and chimpanzees, killing thousands of animals during the last decade in parts of Gabon and RC [ 56 , - ].

Such massive outbreaks in great apes could have major implications for animal conservation. Model of the natural cycle of filovirus. Although many field and laboratory studies have been conducted since the first recorded outbreak in an attempt to identify the reservoir species of MARV and EBOV, conclusive evidence that bats are natural hosts for filoviruses was obtained only recently [ 14 , 45 , - ]. Antibodies and nucleotide sequences specific for ZEBOV [ , ] were detected in the liver and spleen of three fruit bat species in Gabon and RC Hypsignathus monstrosus , Epomops franquetti and Myonycteris torquata , and antibodies and nucleotide sequences specific for MARV [ , ] were found in a fruit bat species in Gabon Rousettus aegyptiacus and in two insectivorous bat species in DRC Rhinolophus eloquens and Miniopterus inflatus.

Finally, a recent study showed that the Luebo outbreak in DRC was linked to massive fruit bat migration, strongly suggesting that humans could be infected directly by bats Fig. Indeed, by their presence in mucosal tissues and skin, these cells are infected early and serve as the substrate for the first replicative viral cycles.

Because of their extensive distribution among the different organs and tissues, and their mobility, dendritic cells and macrophages are probably responsible for viral dissemination and systemic infection [ ]. Intense viral replication then occurs in secondary lymphoid organs and liver, and the virus subsequently spreads to hepatocytes, endothelial cells, fibroblasts and some epithelial cells [ , ]. The pathogenesis of filovirus infection is reviewed in Fig. A model of pathogenesis of filovirus infection, based on findings with Zaire Ebola virus.

Dendritic cells and macrophages are early targets of filoviruses. The virus spreads from the initial site of infection to secondary lymphoid organs and liver where intense replication takes place. Then, other cells are infected such as hepatocytes, endothelial cells, fibroblasts and some epithelial cells. The inhibition of type I interferon IFN production by viral proteins leads to relentless viral replication in most organs. Multifocal necrosis of hepatocytes, liver failure, destruction of secondary lymphoid organs and other tissue damage may result from direct cytopathic effects but also from the host response.

However, despite widespread viral replication, the observed damage to endothelia, liver and other organs is not sufficiently severe to cause terminal shock and death. Endothelial infection is infrequent, occurring in the terminal stages with no clear evidence of cytopathic effects [ 36 ]. Similarly, although multifocal hepatic necrosis may be linked to viral replication in liver, the observed hepatocellular lesions cannot directly lead to death [ , ]. A pathogenic role of the host response is therefore suspected.

In addition, some of these mediators may induce the expression of adhesion molecules at the surface of endothelial cells, so allowing neutrophils and monocytes to invade sites of infection where they may cause bystander tissue damage [ ]. Infected macrophages are involved in the coagulopathy and in the induction of disseminated intravascular coagulation by their abundant expression of tissue factor [ 35 , , ]. A viral protein with superantigen activity might also be involved [ ].

Fatal Ebola haemorrhagic fever is also associated with defective humoral responses, with absent specific IgG and barely detectable IgM [ , ].